NOE fractures in essence are broken nasal bones and cartilages telescoped backward into the interorbital space (Fig. 5.1b) usually as a result of an assault or a motor vehicle accident [6, 7]. The force vector resulting in a NOE fracture is usually transmitted through and thus fracturing five sutures, the frontal process of the maxilla in the place where it joins the internal angular process of the frontal bone, then the medial orbital wall, the infraorbital rim, the lateral nasal wall, and the nasomaxillary suture of piriform aperture (Fig. 5.1c) [8]. The resulting segment (namely, the frontal process of the maxilla, forming the lower two-thirds of medial orbital rim) is the central fragment of the NOE fracture, to which the medial canthal tendon (MCT) is attached. Formation of one or several movable fragments of the medial orbital rim with the attached MCT is the key factor in pathogenesis of NOE fracture.

Classification of NOE fractures is based on the integrity of the central fragment [9]. According to Markowitz et al. [10], there are three types of fractures:

This group of fractures accounts for 18 % of all fractures in this region [11]. Complete bilateral type I NOE fractures resulting in an isolated central fragment, detached from the surrounding osseous structures by all five fracture lines, are more typically an exclusion rather than a rule. It is usually a low-energy unilateral “greenstick” fracture located in the site of the junction of the frontal process of maxilla and the internal angular process of the frontal bone above the MCT attachment site (Fig. 5.1e) [11].

As the central fragment moves downward, it affects the medial palpebral commissure, which causes lengthening of the palpebral fissure and prolapse of the medial canthus. Sagging of the inner infraorbital rim alongside deformation of the piriform aperture is very likely, but it is usually disguised by edema and hematoma of the soft tissues. Injury of the lateral nasal wall causes ipsilateral face asymmetry and obstruction of the lacrimal pathways. Meanwhile, the length of the nasal bridge and intercanthal distance usually do not change, which may give an illusion of the intact NOE complex. In such case, palpating the MCT attachment site or testing central fragment for flexibility under general anesthesia makes diagnosis considerably easier (Fig. 5.1g). Crepitation or flexibility of the bone fragment unmistakably indicates a fracture that requires open repositioning or rigid fixation.

These are moderate-energy fractures that comprise 72 % of all the fractures in this region [11].

Since the only difference between type II and type III fractures is the condition of bones around the MCT attachment site, the respective symptoms are very similar. The detailed clinical presentation of a typical comminuted NOE fracture of both types includes:

Fractures can be either unilateral (the so-called hemi-NOE-fracture) or bilateral (Fig. 5.2b, d). The latter, observed in two-thirds of injured patients, is often asymmetrical and combines types I and II.

Only 10 % of NOE fractures are isolated; more commonly a NOE fracture is a part of the extensive fracture that engages other facial bones or the skull base (Fig. 5.2f) [5, 13, 14]. Fragments of the vomer, ethmoid, and nasal bones may penetrate into the cranial cavity as they are telescoped backward. As a consequence, 50 % of the time this type of fracture involves brain injury; in 40 %, cerebral spinal fluid (CSF) leak; and in 30 %, vision-threatening injuries of the eyeball and optic nerve.¹

A CSF leak is usually caused by propagation of the fracture to the walls of the frontal sinus associated with dura mater rupture. The leak can be detected through visual examination; sometimes a patient himself/herself senses a metallic taste in the nasopharynx. CSF fluid may also gather under the periosteum of the orbital wall either as palpable fluctuating formation or intermittent swelling of orbital tissues worsening at straining and coughing or squeezing of the jugular veins [6].

In 4.5 % of cases, a high-energy fracture of NOE complex is accompanied by a circular fracture of both orbits (3–4 walls), types I and III Le Fort fractures of the zygomatic bones maxilla and mandible that lead to lateral transposition, increase in orbital volume, and divergence of orbits.² Widening of the face, lateral dislocation of both eyeballs, increase in interorbital, interpupillary, and intercanthal distances are the classic signs of traumatic hypertelorism. While this condition accounts for only 1.5 % of all midfacial traumas, the incidence is probably much higher because of the high mortality rate secondary to severe brain injury and other life-threatening injuries caused by the original trauma. In every second patient, injury of the optic nerve causes bilateral blindness. Half of the patients surviving this trauma have bilateral blindness secondary to optic nerve damage. Ruptured globes are often found in these traumas as well [10].

It would not seem difficult to diagnose a NOE fracture for its pathognomonic symptoms such as flattened nasal bridge and telecanthus. However, the difficulty is that in the early days following injury, the obvious signs of fracture are disguised by swelling, ecchymosis, and emphysema of midfacial soft tissues [14, 16].

CSF leak, epistaxis, and epiphora are typical, yet not pathognomonic symptoms. This is where a clinician should be especially suspicious. As bones of the NOE complex endure the load of up to 30 g/cm², any nasal fracture may be a part of a more extensive injury [7]. That is why every midfacial trauma should be treated as a potential NOE fracture.

When making the final diagnosis, CT scanning of 1.5-mm sections is very important (Fig. 5.3) [5, 17]. Axial CT signs indicating a NOE fracture are as follows: spread of the nasomaxillary suture, asymmetrical nasolacrimal ducts, shadowing and destruction of ethmoid air cells, depression and displacement of nasal bones, displaced fracture of the medial orbital wall accompanied by displacement of segments, and orbital emphysema. Coronal CT scans can reveal both inferomedial spread of the nasomaxillary suture and fracture of the infraorbital rim with posterior displacement.

Considering that the overwhelming majority of NOE fractures are very complex, treating them often requires the multidisciplinary approach involving a neurosurgeon, a maxillofacial surgeon, and an ophthalmologist [4, 13].

The treatment begins with stabilization of vital signs and evaluation of the neurological status. The surgical treatment of a NOE fracture can be started only after the risk of penetrating brain injury or open globe injury has been eliminated [18]. In the situation where there is either open brain injury or an open globe, neurosurgical and ophthalmic surgical interventions are performed first, followed by reduction of the NOE fracture.

On condition that the patient’s neurological status is stable, a CSF leak should not prevent early fracture repositioning, because the intervention may stop the leak [6].

The goal of the treatment is to reconstruct the initial appearance of the palpebral fissure and nose, which involves restoration of the intercanthal distance, height, and contour of the nasal bridge and symmetry of medial palpebral commissures [19].

A key to success is an experienced surgeon knowledgeable of the complex midface anatomy, the use and interpretation of appropriate ancillary tests, as well as training in the surgical repair of midfacial trauma [20–23].

Delayed surgical treatment of a NOE fracture is extremely inadvisable because it is much more difficult to eliminate all functional and esthetic problems with late surgery [5, 24, 25] especially with NOE region [7].